Carcinogenesis as a consequence of polycyclic hydrocarbon administration may represent at least in part the end result of an imbalance among several genetically-determined processes occurring with a tissue--activation to epoxides, detoxification of the latter to diols, interaction with macromolecules, i.e., RNA, DNA or protein, conjugation of epoxides with glutathione and the extent of the DNA repair process. Furthermore, the metabolism of polycyclic hydrocarbons is markedly elevated by administration of a number of pollutants, i.e., environmentally-influenced, and the extent of the induction appears also genetically-determined. The objectives of the present proposal are to a) concentrate the activity of the polycyclic hydrocarbon-binding protein from liver and further purify it, b) determine the nature of the interaction of the latter with nuclear components, c) ascertain what is the result of the nuclear expression after such interaction and d) determine if prostaglandins participate in the process of promotion in epidermis.